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AIM: To investigate the presence of the cag-pathogenicity island and the associated histological damage caused by strains with complete cag-PAI and with partial deletions in correlation to the disease status. METHODS: We analyzed the complete cag-PAI of 174 representative Helicobacter pylori (H pylori ) clinical isolates obtained from patients with duodenal ulcer, gastric ulcer, gastric cancer, and non-ulcer dyspepsia using eight different oligonucleOtide primers viz cagA1, cagA2, cagAP1, cagAP2, cagE, cagT, LEC-1, LEC-2 spanning five different loci of the whole cag-PAI by polymerase chain reaction (PCR). RESULTS: The complete screening of the genes comprising the cag-PAI showed that larger proportions of subjects with gastric ulcer (97.8%) inhabited strains with complete cag-PAI, followed by gastric cancer (85.7%), non-ulcer dyspepsia (7.1%), and duodenal ulcer (6.9%), significant differences were found in the percentage distribution of the genes in all the clinical groups studied. It was found that strains with complete cag-PAI were able to cause severe histological damage than with the partially deleted ones. CONCLUSION: The cag-PAI is a strong virulent marker in the disease pathogenesis as it is shown that a large number of those infected with strain with complete cag-PAI had one or the other of the irreversible gastric pathologies and interestingly 18.5% of them developed gastric carcinoma. The presence of an intact cag-PAI correlates with the development of more severe pathology, and such strains were found more frequently in patients with severe gastroduodenal disease. Partial deletions of the cag-PAI appear to be sufficient to render the organism less pathogenic.
METHODS: We analyzed the complete cag-PAI of 174 representative Helicobacter pylori (H pylori) clinical isolates obtained from patients with duodenal ulcer, gastric ulcer, gastric cancer, and non-ulcer dyspepsia using eight different oligonucletide primers viz cagA1, cagA2, cagAP1, cagAP2, cagE, cagT, LEC- 1, LEC- 2 spanning five different loci of the whole cag-PAI by polymerase chain reaction (PCR). RESULTS: The complete screening of the genes comprising the cag-PAI showed that the proportions of subjects with gastric ulcer (97.8%) inhabited with complete cag-PAI , followed by gastric cancer (85.7%), non-ulcer dyspepsia (7.1%), and duodenal ulcer (6.9%), significant differences were found in the percentage distribution of the genes in all the clinical groups studied. It was found that with with cag-PAI were able to cause severe histological damage than with the partially deleted ones. CONCLUSION: The cag-PAI is a strong virulent marker in the disease pathogenesis as it is shown that a large number of those infected strain with complete cag-PAI had one or the other of the irreversible gastric pathologies and interestingly 18.5% of them developed gastric carcinoma. The presence of an intact cag-PAI correlates with the development of more severe pathology, and such Danish were found more more frequently in patients with severe gastroduodenal disease. Partial deletions of the cag-PAI appear to be sufficient to render the organism less pathogenic.